Fractures In Diabetic Patients Research Articles

The association of serum 25-hydroxyvitamin D and vertebral fractures in patients with type 2 diabetes

Vitamin D is an important regulator of bone health. Previous studies examining the association between vitamin D deficiency and osteoporotic fractures have reported conflicting results. The relationship between vitamin D status and risk of vertebral fractures in diabetic patients is unknown. The objective of this study was to examine whether low serum 25-hydroxyvitamin D [25(OH)D] levels were associated with vertebral fractures in patients with type 2 diabetes. This cross-sectional study was conducted among 161 postmenopausal women and 180 men with type 2 diabetes. Serum concentrations of 25(OH)D were measured and the presence of vertebral fracture was assessed using lateral plain radiographs of the thoracolumbar spine. Women had lower 25(OH)D levels than men (31.3 ± 17.7 vs. 41.3 ± 26.5 ng/mL, p<0.001). Vertebral fractures were found in 16% of patients. Men with a serum 25(OH)D concentration greater than 30 ng/mL showed a lower prevalence of vertebral fractures compared to those with 20-29.9 ng/mL or those with less than 20 ng/mL (9.4% vs. 17.9% vs. 21.7%, p for trend=0.036). However, there was no significant association between vitamin D status and the prevalence of vertebral fractures in women (14.4% vs. 19.2% vs. 26.6%, p for trend=0.111). After adjusting for multiple confounding factors, men with a serum 25(OH)D concentration of less than 20 ng/mL were associated with an increased risk of vertebral fractures (OR 7.87; 95% CI 1.69-36.71), but not women. In conclusion, serum 25(OH)D levels below 20 ng/mL were associated with an increased vertebral fracture risk in men with type 2 diabetes.

FRAX Tool Badly Underestimated Diabetics’ Fracture Risk in Study

SAN DIEGO – The World Health Organization's widely used, Web-based fracture risk assessment tool, known as FRAX, seriously underestimates the risk of major osteoporotic and hip fractures in patients with diabetes, according to a large Canadian study. This finding indicates diabetes is a risk factor for fractures beyond those in the FRAX tool, which include age, gender, smoking, fracture history, and glucocorticoid use – but not diabetes. “One implication of our findings is that FRAX should be applied cautiously in clinical situations involving diabetic patients,” Lora Giangregorio, Ph.D., said at the annual meeting of the American Society for Bone and Mineral Research. “Future iterations of the FRAX tool might consider adding diabetes to the list of risk factors,” added Dr. Giangregorio of the University of Waterloo (Ontario). She presented an analysis of a database from 3,518 patients with type 1 or type 2 diabetes and 36,085 nondiabetic controls, all at least 50 years old when they underwent bone-density testing during 1987–2008. She and six coauthors subsequently published the study online in the Journal of Bone and Mineral Research (DOI: 10.1002/jbmr.556). FRAX was used to calculate 10-year fracture-risk probabilities, and the actual incidence of major osteoporotic or hip fractures was determined through 2008. The key finding: After the researchers controlled for FRAX fracture probability scores and the use of osteoporotic medications, diabetes was independently associated with a 59% increased fracture rate during an average 10 years of follow-up. Of note, despite the increased fracture rate documented in diabetic patients in this study, a lower proportion of subjects with diabetes were receiving osteoporotic medications, compared with the nondiabetes population, Dr. Giangregorio observed. Diabetes was a stronger predictor of hip fracture risk in the younger study participants. Indeed, it was independently associated with a 5.3-fold increased risk of hip fracture in individuals younger than age 65, compared with a 2.1-fold increase in those who were older. In contrast, the risk of major osteoporotic fractures in diabetic patients was not related to age. An important area for future research, in Dr. Giangregorio's view, is whether some diabetes medications are associated with an increase in fractures while others are not. In another study presented at the meeting, Dr. Ling Oei of Erasmus University, Rotterdam, the Netherlands, noted that patients with type 2 diabetes are paradoxically at increased risk of osteoporotic fractures even though their bone mineral density is typically normal or even higher. In a prospective, population-based study of 203 patients with adequately controlled type 2 diabetes, 217 others with inadequately controlled disease, and 3,715 nondiabetic controls, Dr. Oei and coworkers showed that women with inadequately controlled diabetes had significantly higher bone mineral density at both the lumbar spine and femoral neck, but a 1.6-fold increased risk of fracture during an average 8.2-year follow-up. Dr. Giangregorio and Dr. Oei reported having no financial conflict.

Clinical Aspects of Diabetic Bone Disease: An Update

Older adults with type 2 diabetes have a higher risk of fracture but do not have decrements in bone density. The reasons for greater bone fragility in diabetes are still not clearly understood, but progress has been made in identifying potential contributors. With new imaging techniques, increased cortical porosity has been identified as a possible contributing factor to bone fragility. Cortical porosity may be especially detrimental to bone strength in the presence of higher levels of advanced glycation end products. Initial results have reported higher levels of marrow adiposity in diabetic men, suggesting that diabetes may contribute to marrow stem-cell lineage allocation toward adipocytes rather than osteoblasts. Higher levels of sclerostin have also been observed in diabetic patients, indicating that osteocyte function may play a role in diabetic bone. An important clinical question, “How to best predict fracture in diabetic patients?” has been addressed with studies demonstrating that BMD T-score and FRAX score predict fractures but underestimate absolute risk in diabetic patients. For prevention of fractures, there is now evidence from a clinical trial that intensive glycemic control does not increase fracture or fall risk but also does not reduce these outcomes. The pursuit of these new findings promises to provide insights into the reasons for greater fragility of diabetic bone and the best methods for fracture prevention in this population.

MRI of the cuboid bone: Analysis of changes in diabetic versus non-diabetic patients and their clinical significance

Objectives(1) To investigate the association between diabetes and marrow changes in the cuboid; and (2) to evaluate the influence of age, gender, body mass index (BMI) and use of insulin in the occurrence of marrow changes in the cuboid. Research design and methodsMR and X-ray foot examinations of 237 patients [94 males, 143 females; mean age, 47.1 years (range 16–93 years)], five of whom underwent bilateral examinations, were reviewed. MR and radiographic studies were analyzed for the presence of marrow edema and fractures in the cuboid. Findings were correlated with demographic data (age, gender) and clinical information (BMI and use of insulin). ResultsTwo hundred and forty two feet – 69 diabetic and 173 non-diabetic – were retrospectively evaluated. There was a higher prevalence of marrow edema and fractures in the diabetic cuboid (n=31, 45%) compared to non-diabetic cuboid (n=25, 14%, p=0.02). A fracture line was seen in fourteen (20%) diabetic cuboid bones compared to 4 (2%) in non-diabetic cuboid bones (p<0.0001). Eleven (79%) cases of cuboid fractures in the diabetic population were radiographically occult. Multivariate data analysis revealed an adjusted odds ratio of 4.416 (95% CI; 2.307, 8.454) for the relationship between marrow changes (edema and fractures) in the cuboid and diabetes. For each year of age, the odds of changes in the cuboid increased by 2.2% (95% CI; 1.001, 1.044). ConclusionDespite not bearing weight, the cuboid bone is more vulnerable to marrow edema and fractures in diabetic patients compared to non-diabetic patients. Age seems to be an influential factor.

Thiazolidinediones and bone fractures.

Thiazolidinediones and bone fractures.

Mortality after Hip Fracture in Diabetic Patients

Type 2 diabetic patients have an increased incidence of hip fracture. In this study, we aimed to evaluate the mortality rate after hip fracture and determine the predictors of mortality in diabetic patients. 356 patients who sustained a hip fracture between January 1997 and June 2008 were retrospectively reviewed for the study. Of the eligible 230 patients, 69 had type 2 diabetes. Each of these patients' medical and nursing notes were reviewed to ascertain additional information, including patient demographic factors, prior co-morbidities, fracture type, length of post-fracture stay and post-operative complications, the presence and duration of diabetes, glucose levels, HbA1c levels, albumin and hemoglobin levels. 148 women (64.3%) and 82 men (35.7%) were included in the study. The mean age of the study group was 76.1 ± 10.4 years. The mean age for diabetics was 76.1 ± 12.0 years and was 75.1 ± 9.4 years for non-diabetics ( P=0.343). Diabetic patients with hip fracture had a higher risk of mortality than the non-diabetic patients. One year survival probabilities of diabetic and non-diabetic patients were respectively 68.0% and 87.3% (p=0.033). In diabetic patients with a hip fracture, predictors of mortality were advanced age, the presence of postoperative complications and elevated HbA1c levels. Diabetic patients have an increased risk of mortality after hip fracture. The medical care in the post-operative period, including glycemic control and postoperative complications, should be optimized in diabetic patients suffering from hip fracture in order to decrease mortality in these patients.

Osteoporosis and risk of fracture in patients with diabetes: an update

Diabetes mellitus (DM) and osteoporotic fractures are two of the most important causes of mortality and morbidity in older subjects. Recent data report a close association between fragility fracture risk and DM of both type 1 (DM1) and type 2 (DM2). However, DM1 is associated with reduced bone mineral density (BMD), whereas patients with DM2 generally have normal or increased BMD. This apparent paradox may be explained by the fact that, at a given level of BMD, diabetic patients present lower bone quality with respect to non-diabetics, as shown by several studies reporting that diabetes may affect bone tissue by means of various mechanisms, including hyperinsulinemia, deposition of advanced glycosylation endproducts (AGEs) in collagen, reduced serum levels of IGF-1, hypercalciuria, renal failure, microangiopathy and inflammation. In addition, the propensity to fall and several comorbidities may further explain the higher fracture incidence in DM patients with respect to the general population. It is reasonable to expect that close metabolic control of diabetes may improve bone status, although its effect on reduction of fracture risk has not yet been demonstrated. However, metformin has a direct effect on bone tissue by reducing AGE accumulation, whereas insulin acts directly on osteoclast activity, and thiazolidinediones (TZD) may have a negative effect by switching mesenchymal progenitor cells to adipose rather than bone tissue. New prospects include the incretins, a class of antidiabetic drugs which may play a role linking nutrition and bone metabolism. Better knowledge on how diabetes and its treatments influence bone tissue may lie at the basis of effective prevention of bone fracture in diabetic patients. Thus, close glycemic control, adequate intake of calcium and vitamin D, screening for low BMD, and prevention and treatment of diabetic complications are key elements in the management of osteoporosis in both DM1 and DM2. Attention should be paid to treating diabetes with TZD in women with DM2, particularly if elderly. Lastly, patients with osteoporosis and diabetes should be offered the same pharmacological treatments as non-diabetics, although specific trials on the effects of anti-osteoporotic drugs in the diabetic population are lacking.

Osteoporosi nei pazienti con diabete mellito

Summary Introduction Diabetes mellitus (DM) and osteoporotic fractures are major causes of mortality and morbidity in older subjects. Recent reports have revealed close association between fracture risk and DM types 1 and 2 (DM1 and DM2, respectively). Aim of this review is to highlight the importance of these diseases in the elderly and examine certain etiopathogenetic aspects of DM-associated osteoporosis, which could be useful in management of diabetic patients. Materials and methods We searched the Embase and PubMed databases using diabetes, osteoporosis, and bone mineral density (BMD) as search terms and 1989-2009 as publication dates. Discussion The risk of fractures seems to be increased in both types of DM although DM2 seems to be associated with normal-high BMDs compared with the normal population. This apparent paradox could reflect greater bone frailty in diabetic patients that are unrelated to adipose tissue, hyperinsulinemia, deposition of advanced glycosylation end products in collagen, reduced serum IGF-1 levels, hypercalciuria, renal failure, microangiopathy, and/or inflammation. Diabetic patients’ propensity to fall and multiple comorbidities might also explain their higher fracture rates. The effects of drugs that inhibit bone resorption in diabetic patients are probably similar to those obtained in nondiabetics although there is little information on this issue. In general, effective treatment of diabetes has positive effects on bone metabolism. Metformin acts directly on bone tissue, reducing AGE accumulation, and insulin has direct effects on osteoclast activity. In contrast, the thiazolidinediones seem to have negative effects since they orient mesenchymal progenitor cell differentiation toward adipose rather than bone tissue. Incretin therapy is a newer approach that appears to modify interactions between nutrition and bone turnover (e.g., postprandial suppression of bone resorption). Conclusions Better understanding of how diabetes and its treatment influence bone tissue could lead to more effective strategies for preventing fractures in diabetic patients. More investigation is needed to determine whether conventional osteoporotic therapy is fully effective in patients with DM.

Early Complications Following the Operative Treatment of Pilon Fractures with and without Diabetes

An increased rate of complications has been clearly shown in diabetic patients undergoing operative treatment for displaced ankle fractures. To date, no studies have specifically looked at the complication rates following the operative management of pilon fractures in this difficult patient population. We performed a retrospective review to determine the rates of complications in diabetic patients undergoing operative fixation of tibial pilon fractures compared with a control group of patients without diabetes. The trauma registry was utilized to identify all patients who underwent primary treatment for a tibial pilon fracture between January 2005 and June of 2007 at a single Level 1 trauma center. A minimum of 6-month followup was required for inclusion. A chart and radiographic review was completed to identify the complications seen in each patient population. Specifically, we looked at the rate of infection (superficial and deep), the rate of nonunion or delayed union, and the rate of surgical wound complications. A total of 14 fractures in 13 diabetic patients, and 69 fractures in 68 non-diabetic patients met inclusion criteria. In the diabetic patient group, the average age was 48 years, the average BMI was 35, and 36% of the fractures were open. In the non-diabetic group, the average age was 47 years, the average BMI was 29, and 35% of the fractures were open. Only the difference in BMI was statistically significant. The infection rate was 71% for diabetic patients (43% deep infection), and 19% for non-diabetic patients (9% deep infection) [p < 0.001, odds ratio 10.719 (95% confidence interval 2.914 to 39.798)]. Overall, the rate of non-union/delayed union was 43% in the diabetic group versus 16% in the non-diabetic group [p = 0.02, odds ratio 3.955 (95% confidence interval 1.145 to 13.656)]. The rate of surgical wound complications was 7% in both the non-diabetic and diabetic patient groups. The management of tibial pilon fractures in diabetic patients is difficult, with a high rate of complications compared to non-diabetic patients. These results mirror those previously reported for ankle fractures in diabetic patients.

The risk of osteoporosis-related fracture in diabetic patients

The risk of osteoporosis-related fracture in diabetic patients

Open Calcaneal Fractures in Diabetic Patients with Neuropathy: A Report of Three Cases and Literature Review

Level of Evidence: V, Case Report

The Management of Ankle Fractures in Patients with Diabetes

Patients with diabetes mellitus have higher complication rates following both open and closed management of ankle fractures. Diabetic patients with neuropathy or vasculopathy have higher complication rates than both diabetic patients without these comorbidities and nondiabetic patients. Unstable ankle fractures in diabetic patients without neuropathy or vasculopathy are best treated with open reduction and internal fixation with use of standard techniques. Patients with neuropathy or vasculopathy are at increased risk for both soft-tissue and osseous complications, including delayed union and nonunion. Careful soft-tissue management as well as stable, rigid internal fixation are crucial to obtaining a good outcome. Prolonged non-weight-bearing and subsequently protected weight-bearing are recommended following both operative and nonoperative management of ankle fractures in patients with diabetes.

Increased Risks of Hip Fracture in Diabetic Patients of Taiwan

Using Taiwan's National Health Insurance claim data, we evaluated the age-, sex-, and urbanization-specific incidence density and relative risks of hip fracture in the diabetic population. Diabetic patients (n = 500,868) and an age- and sex-matched control group (n = 500,248) were linked to inpatient claims (1997-2002) to identify hospitalizations for nontransport accident hip fracture. The person-year approach with Poisson assumption and Kaplan-Meier analysis were used to estimate the incidence and the cumulative event rates. We also assessed the age-, sex-, and urbanization-specific relative risks of hip fracture in relation to diabetes with the Cox proportional hazard regression model. The overall incidences of hip fracture for diabetic men and women, respectively, were 3.01 and 6.75/1,000 person-years, which were higher than those for control men and women. There were significant interactions of diabetes and age and diabetes and urbanization statuses. Hazard ratios (HRs) of diabetic patients aged 35-44 years (men 2.45 [95% CI 1.65-3.64]; women 3.19 [1.39-7.33]) were higher than those of diabetic patients aged 55-64 years (men 1.90; women 2.81), but in diabetic men aged >74 years and diabetic women aged >84 years, the HRs were compared with null statistically (HRs 0.98 and 0.91, respectively). Diabetic patients living in rural areas tended to have higher HRs of hip fracture. In Taiwan, diabetes increased the risk of hip fracture in both sexes in all age-groups except in diabetic men aged >74 years and diabetic women aged >84 years. Higher HRs of hip fracture were disproportionately observed in younger diabetic patients and in those living in rural areas.

Bone Mineral Density Is not Sensitive Enough to Assess the Risk of Vertebral Fractures in Type 2 Diabetic Women

Although the association between diabetes and osteoporosis has been studied, it remains unclear if the pathogenesis of vertebral fractures in patients with type 2 diabetes would be similar to those without diabetes. One hundred and fifty female diabetic patients without apparent proteinuria as well as 716 women without diabetes (control group) were examined by lateral thoracic and lumbar spine radiographs as well as dual-energy X-ray absorptiometry. Vertebral fractures were found in 26 (17.3%) and 158 (22.1%) subjects in the diabetic and control groups, respectively. Diabetic patients had higher absolute and age-matched (Z score) values of lumbar bone mineral density (L-BMD) than controls despite their significantly higher mean age. By receiver operating characteristic (ROC) analysis, the absolute L-BMD values for detecting vertebral fractures were higher and sensitivity and specificity were lower in diabetic patients than controls (0.816 g/cm2 vs. 0.716 g/cm2 and 66.0% vs. 74.8%, respectively). Logistic regression analysis adjusted for age, body weight, and height also showed that L-BMD was not significantly associated with the presence of vertebral fractures in diabetic patients (odds ratio [OR] = 0.61, 95% confidence interval [CI] 0.34-1.09 per standard deviation increase, P = 0.0954), in contrast to the significant association in controls (OR = 0.23, 95% CI 0.16-0.33, P < 0.0001). These results show that L-BMD is not sensitive enough to assess the risk of vertebral fractures in female diabetic patients and suggest that bone fragility not defined by BMD might be related to the risk of vertebral fractures in them.

Outcome In Ankle Fractures In Diabetic Vs Non- Diabetics

Background: Ankle fractures in diabetic patients have always been considered difficult injuries and previous studies in this field showed that the incidence of complication can be in the range of 32%3 to 42.3%6. Aims: The aim of this study was to assess the outcome in ankle fractures in diabetic population and to find out reasons for any results contrary to previous studies. Methods: We performed a case control study comparing a group of 24 diabetic patients, with ankle fractures, with a group of 48 non-diabetic patients demographically similar for age, gender, type of injury, treatment provide and length of follow-up. In diabetic group 9 were treated conservatively and 15 had ORIF while in non-diabetic group 16 were treated conservatively and 32 underwent operative treatment. The diabetic and non-diabetic groups were followed up for mean periods of 50.3 months and 43.1 months respectively and on the conclusion of the study a clinic was arranged in April 2003 and the outcome was assessed according to the 100 point Maryland foot score. Results: In the diabetic group 4 patients while in the non-diabetic group 7 patients developed complications. None of the 72 patients in this study required further surgery. The mean Maryland foot score of diabetic group was 95.08 and that of nondiabetic group was 93.79. Conclusion: Our study shows that in the presence of optimal control of diabetes mellitus and careful patient selection for type of treatment, these lesions can result in an outcome comparable to non-diabetic patients with similar injuries (p = 0.086).

Possible participation of advanced glycation end products in the pathogenesis of osteoporosis in diabetic patients

Osteoporosis, one of the most prevalent metabolic bone diseases in developed countries, is a major public health problem through its association with fragility fractures. Several epidemiological studies have reported moderately increased risks of osteoporotic bone fractures in diabetic patients compared with general population. However, the underlying molecular link between diabetes and osteoporosis remains to be elucidated. In diabetes mellitus, the formation and accumulation of advanced glycation end products (AGEs) progress. There is a growing body of evidence to show that AGEs-their receptor (RAGE) interactions are involved in the development of atherosclerosis and diabetic microangiopathy. AGEs enhance osteoclast-induced bone resorption in cultured mouse unfractionated bone cells. Furthermore, we have recently found that AGEs-RAGE interactions induced human mesenchymal stem cell apoptosis and subsequently prevented cognate differentiation into adipose tissue, cartilage, and bone. In vivo, serum levels of AGEs are elevated in patients with osteoporosis as well. These observations let us to hypothesize that AGEs could explain the molecular link between diabetes and osteoporosis. In this paper, we would like to propose the possible ways of testing our hypotheses. Does treatment with metformin, which has a potential effect on the inhibition of glycation reactions in vivo, decrease the risk for osteoporotic bone fractures in diabetic patients? If the answer is yes, is this beneficial effect of metformin superior to that of other anti-diabetic agents with equihypoglycemic properties? Does treatment with pyridoxamine, a post-Amadori inhibitor (so-called Amadorins) of AGE formation, reduce the risk for osteoporotic bone fractures as well? Furthermore, are increased levels of AGEs and RAGE in bone tissues associated with high risk for bone fractures in patients with diabetes? These clinical studies could clarify whether the AGEs-RAGE interactions serve as a causal link between diabetes and osteoporosis.

Diabetic osteopathy

The aim of this study was to point out some dilemmas about the existence and pathogenesis of primary diabetic osteopathy as a separate entity, based on currently available studies. Expert disagreements are present not only about the occurrence of generalized osteopathy with diabetic disease, but also about direct relationship between metabolic diabetes control and bone metabolism and influence of disease duration and sex on bone changes. Decreased bone formation is the basic mechanism leading to decreased bone mass. Biochemical markers showed no clear connection with bone density measurement. Insulin and insulin-like growth facotr (IGF) affect bone metabolism. OSTEOPATHY IN PATIENTS WITH DIABETIC DISEASE-TYPE1: Some clinical studies have shown that patients with diabetic disease-type have a mild decrease in bone mass, while others have not presented such results. OSTEOPATHY IN PATIENTS WITH DIABETIC DISEASE-TYPE2: In patients with diabetic disease-type 2 the risk for osteopathy is even less defined. Patients treated with oral hypoglycemics present with higher decrease of bone mass has than patients treated with insulin therapy. This could partly be explained by anabolic effects of insulin on bones. Literature data are contradictory concerning the occurrence of bone fractures in diabetic patients. A survey of bone fracture occurrence in diabetic patients was performed in "Veljko Vlahović Medical Center" in Vrbas and it included a group of 100 patients with diabetic disease. The results show that 12 patients had some fractures: mostly females in postmenopause, aged and with secondary insulin-dependent diabetes and most frequently arm fractures. Considering contradictory literature data, further longitudinal studies are necessary.

A protocol for treatment of unstable ankle fractures using transarticular fixation in patients with diabetes mellitus and loss of protective sensibility.

Surgical treatment of ankle fractures in patients with diabetes mellitus is associated with a high complication rate. Diabetic patients with peripheral neuropathy are a particularly difficult group to treat because of their inability to sense deep infection, repeat trauma, and wound complications. The purpose of this study was to evaluate a protocol that included transarticular fixation and prolonged, protected weightbearing in the treatment of unstable ankle fractures in diabetic patients with peripheral neuropathy and loss of protective sensibility. The authors retrospectively reviewed the records of 15 patients with diabetes mellitus, unstable ankle fractures (AO classification 44B), and loss of protective sensibility confirmed via testing with a 5.07 Semmes-Weinstein monofilament. Retrograde transcalcaneal-talar-tibial fixation using large Steinmann pins or screws in conjunction with standard techniques of open reduction and internal fixation was used. The postoperative treatment protocol included: 1) short leg, total contact casting and nonweightbearing status for 12 weeks; 2) removal of the intramedullary implants between 12 and 16 weeks; 3) application of a walker boot or short leg cast with partial weightbearing for an additional 12 weeks; and 4) transition to a custom-molded ankle-foot orthosis (AFO) or custom total-contact inserts in appropriate diabetic footwear. The major complication rate for all fractures was 25% (4/16) and for closed fractures was 23% (3/13). These are lower than previously reported rates between 30% (3/10) and 43% (9/21) for diabetic patients with and without neuropathy. The amputation rate for all fractures was 13% (2/16) and for closed fractures alone was 8% (1/13). These are similar to previously reported rates of 10% (2/10) to 20% (2/21). There were no deaths or Charcot malunions in this series. The combination of transarticular fixation and prolonged, protected weightbearing provided 13 of 15 patients with a stable ankle for weightbearing. Although these fractures remain a treatment challenge, this study presents a successful, multidisciplinary protocol for treatment of unstable ankle fractures in the most challenging group of diabetic patients - those with loss of protective sensibility.

Bone Mineral Density and Bone Metabolism in Diabetes Mellitus

The effect of diabetes mellitus on bone metabolism and bone mineral density is discussed controversially. Diabetes mellitus due to an autoimmune process seems to be associated with low turnover osteopenia either in the animal model or in children and adolescents. A number of factors are discussed as being involved, but in this age group clinical symptoms are missing. Adult patients of either sex with IDDM show a reduced bone mineral density when measured at peripheral sites such as the distal forearm or the femoral neck, diabetic complications such as neuropathy and microangiopathy seem to pronounce the deficit of bone mass. In these patients, osteopenia is accompanied by a high turnover situation of bone metabolism, possibly due to microvascular complications. In contrast, patients with NIDDM and here especially overweight women have a normal or even increased bone mineral density. Up to now, there is no convincing evidence for an increased incidence of osteoporotic fractures in diabetic patients. Systemic diabetic osteopenia therefore does not seem to be of great epidemiological relevance.

Fractures and dislocations of the foot and ankle in diabetics associated with Charcot joint changes.

This study was undertaken to evaluate the occurrence of Charcot joint changes in diabetic patients after fractures and/or dislocations of the foot and ankle. There were 20 fracture/dislocations of the foot and ankle in 18 patients, with an average follow-up of 27 months (range 14-70 months). There were eight fractures of the midfoot, six fractures of the ankle, four fractures of the hindfoot, and two fractures of the forefoot. Eight fractures were followed by the development of Charcot changes: five in the midfoot and one each in the forefoot, hindfoot, and ankle. Of nine fractures recognized early and initially treated by early immobilization or ORIF, seven healed uneventfully. Two fractures, both open injuries, developed soft tissue infection and osteomyelitis, respectively. Of the 11 fractures in which there was a delay in diagnosis and treatment, eight developed Charcot changes. The early recognition and appropriate treatment of fractures in diabetic patients appears to be important in the prevention of Charcot joint changes.